Polycystic Ovary Syndrome

Introduction to polycystic ovary syndrome Polycystic ovary syndrome is an endocrine disease in which the ovary is enlarged and contains many fluid-filled sacs with elevated androgen levels and inability to ovulate. The most striking feature is anovulation. basic knowledge The proportion of illness: 0.09% Susceptible people: good for women Mode of infection: non-infectious Complications: endometrial cancer, hypertension, breast cancer

The cause of polycystic ovary syndrome

Genetic factors (30%):

PCOS is an autosomal dominant inheritance, or X-linked (associated) inheritance, or a disease caused by a genetic mutation. Most patients have a karyotype of 46, XX, and some patients have chromosomal aberrations or chimeric types such as 46, XX. /45, XO; 46, XX/46, XXq and 46, XXq, PCOS originated from pre-pubertal adrenal gland disease, that is, when stimulated by intense stress, the reticular band secretes excessive androgen and is converted to estrone outside the gonads. Feedback-induced GnRH-GnH release rhythm disorder in HP axis, LH/FSH ratio increased, secondary to increased ovarian androgen production, that is, adrenal and ovary secrete more androgen to cause hyperandrogenism, hyperandrogen blood The disease causes thickening of the fibrosis in the ovary, inhibits follicular development and eggs, and causes cystic enlargement of the ovary and chronic anovulation.

Abnormal gonadotropin release (30%):

In patients with PCOS, blood LH is elevated, while FSH is normal or decreased. LH/FSH is 2 to 3. LH may be overreactive after intravenous injection of GnRH, suggesting that it may be primary hypothalamic-pituitary dysfunction, dopaminergic energy in the hypothalamus. The opioid peptide nerve can inhibit the inhibition of GnRH neurons, which can lead to an increase in LH secretion, but it is more likely to be caused by abnormal feedback inhibition of estrogen. The non-cyclical extra-adeno-estrogened estrogen (estrone E1) will Lead to positive feedback on LH secretion and negative feedback inhibition on FSH secretion. LH stimulates follicular cell proliferation, produces a large number of androgens, and androgen cannot be completely converted into estrogen, further increasing the production of extracellular aromatized E1, excessive androgen Follicular atresia, ovarian envelope fibrosis and thickening of the capsule, due to lack of LH peak in the middle of the menstrual cycle, ovulation disorders, in addition, it has been found that PCOS patients' ovaries may also secrete "inhibin", inhibit the secretion of FSH, affect The follicles are mature and have more vesicular follicles. In recent years, hyperinsulinemia and increased IGF have also increased LH secretion.

Too much androgen (30%):

In PCOS, almost all androgen production is increased, while sex hormone binding globulin (SHBG) is reduced, free androgen is increased, activity is enhanced, and too much androgen is derived from ovary or adrenal gland, and high dose GnRH is excited. The agent reduces gonadotropin, androstenedione and testosterone, but has no effect on DHEAS derived from the adrenal gland. It is reported that about 70% of PCOS patients are caused by ovarian-derived androgens: 1 due to steroid hormones required enzyme system Dysfunction, such as aromatase deficiency, 3-ketoxime dehydrogenase deficiency or decreased activity, abnormal regulation of P45OC17A, estrogen synthesis disorder, a large number of androgens converted to estrone in the periphery (fat, liver, kidney), also It is believed that the ovarian development is insufficient to decrease the activity of aromatase, the 2LH pulse frequency and amplitude increase, stimulate the formation of follicular cells and interstitial cells and androgen production, excessive androgen promotes follicular atresia, and early ovarian granulosa cells are yellowed. , growth stops, can not ovulate, form PCOS.

Prevention of polycystic ovary syndrome

The exact cause of pcos is still unclear. The occurrence of pcos is closely related to genetic factors, environmental factors, and lifestyle. For example, parents have diabetes, hypertension, and family history of parental alopecia; low birth weight at birth; pubic hair before 8 years old Appears; girls who are overweight and have acne; puberty obese girls, life factors.

Polycystic ovary syndrome complications Complications endometrial cancer hypertension breast cancer

Can be complicated by endometrial cancer, type 2 diabetes, hypertension, cardiovascular disease and so on.

1. Tumor: persistent, non-periodic, relatively high estrogen levels and elevated E1 and E1/E2 ratios to endometrial stimulation, no progesterone resistance, endometrial cancer and breast cancer The incidence rate increases.

2, cardiovascular disease: dyslipidemia, easy to cause atherosclerosis, leading to coronary heart disease, high blood pressure and so on.

3, diabetes: insulin resistance and hyperinsulinemia, obesity, easy to develop into recessive diabetes or diabetes.

4, hemorrhoids: excessive secretion of facial sebum caused by hairy.

5, infertility: due to amenorrhea does not ovulation.

Symptoms of Polycystic Ovary Syndrome Common Symptoms Menstrual Delayed Follicles Increase Abortion Polycystic Ovary Occurrence of Laryngeal Hair Hyperplasia Facial Hair Clear Amenorrhea Dysmenorrhea Menopause

1, menstrual abnormalities: menstrual scarcity, amenorrhea, a small number of functional uterine bleeding, mostly occurred in adolescence, irregular menstruation after menarche, sometimes accompanied by dysmenorrhea.

2, hairy: more common, the incidence can reach 69%, due to elevated androgen, visible upper lip, lower jaw, chest, back, lower abdomen in the middle, upper thighs and perianal mane thickening, increased, but hairy The degree is not proportional to the level of androgen (receptor number, estrogen, SHBG and hair follicles and other factors affecting androgen sensitivity), and may be accompanied by hemorrhoids, excessive secretion of facial sebum, low voice, clitoris hypertrophy, There are signs of masculinization such as larynx.

3, infertility: due to long-term non-ovulation, patients with infertility, sometimes occasional ovulation or abortion, the incidence of up to 74%.

4, obesity: body weight more than 20%, body mass index 25 accounted for 30% to 60%, obesity mostly concentrated in the upper body, waist / hip ratio > 0, 85, more from the beginning of puberty, gradually increasing with age.

5, ovarian enlargement: a small number of patients can be touched by general gynecological examination, the tough ovary, most need to be confirmed by auxiliary examination.

6, estrogen effect: all patients showed good estrogen effect, when examined, the amount of cervical mucus can be seen, sustained, a large number of estrogen effects can occur intimal hyperplasia, atypical hyperplasia, and even cancer.

Examination of polycystic ovary syndrome

First, hormone determination

(A) gonadotropin: about 75% of patients with elevated LH, PSH normal or decreased, LH / FSH 3.

(B) steroid hormone

1. Androgen, including testosterone, dihydrotestosterone, androstenedione and 17 ketosteroids, elevated free androgen due to decreased SHBG.

2, the total amount of estrogen can reach 140pg / ml, androgen equivalent to the early stage of follicles about 60pg / ml, the formation of extragonadal estrone increased E1/E2 1.

3, the adrenal DHEAS production increased, plasma concentration 3.3g / ml, 17 hydroxyprogesterone also increased (normal laparoscopic, to directly observe ovarian morphology or biopsy, puncture, wedge cutting and electrocautery treatment.

Second, CT and magnetic resonance

To identify and exclude pelvic tumors.

Third, laparotomy

It is performed when a ovarian tumor is to be diagnosed or when an ovarian wedge is to be performed.

1, LH / FSH: blood LH and FSH ratio and concentration are abnormal, non-periodic secretion, LH increased in most patients, and FSH is equivalent to early follicular phase, LH / FSH 2.5 ~ 3, many scholars believe that LH The increase in /FSH ratio is characteristic of PCOS.

2, male steroids: excessive androgen, testosterone, androstenedione, DHEA, DHEAS levels can be increased.

3, female steroids: estrone and estrogen abnormalities, constant estrogen levels, E2 levels of fluctuations, no normal menstrual periodic changes, E1 levels increased, E1/E2>1.

4, PRL: PCOS can be slightly elevated, but due to hyperprolactinemia can appear PCOS symptoms, should be identified.

5, urine: 17-OHCS and 17-KS 24h urine 17-ketone rise reflects the increase in adrenal androgen secretion.

6, dexamethasone inhibition test: can inhibit the secretion of adrenal hormones, take dexamethasone 0.5mg, every 6 hours, a total of 4 days, take blood samples after taking, such as serum dehydroepiandrosterone sulfate or urinary 17-ketone Steroids are inhibited to normal levels, which may rule out the possibility of adrenal tumors or hyperplasia.

7, chorionic gonadotropin (HCG) stimulation test: HCG can stimulate the synthesis of androgen in the ovary, injection of HCG can cause elevated plasma androgen levels.

8, corticotropin (ACTH) stimulation test: ACTH stimulation test can promote adrenal gland androgen DHEA and urine 17-KS increased.

Through the HCG stimulation test, the dexamethasone suppression test, the ACTH stimulation test can help identify the source of androgen elevation.

9, vaginal exfoliation cell maturity index: is a simple way to understand the status of sex hormones in the body, smear of excessive testosterone often appears in the form of three layers of cells at the same time, the number of cells in the three layers is almost equal, but must be associated with inflammation The difference, estrogen levels can be estimated from the percentage of superficial cells, but does not reflect the amount of hormones in the blood.

10, basal body temperature measurement: to determine whether there is ovulation, ovulation is biphasic, non-ovulatory is generally single-phase type.

Fourth, the impact check

1, pelvic B-ultrasound: ovarian enlargement, at least 10 or more 2 ~ 6mm diameter follicles per plane, mainly distributed in the periphery of the ovarian cortex, a few scattered in the interstitial, interstitial increased.

2, pneumonia film: bilateral ovarian enlargement 2 to 3 times, if the main source of androgen is the adrenal gland, the ovary is relatively small.

3, laparoscopic (or surgery): see ovarian shape is full, the surface is pale and smooth, the capsule is thick, sometimes visible under the capillary network, because the appearance of the color is pearl-like, commonly known as oyster ovary, the surface can be seen multiple cystic follicles .

4, transvaginal high-resolution ultrasound examination of the ovaries, making the diagnosis of PCOS a breakthrough, at present, experienced doctors have done this examination has become the basis of diagnosis, transvaginal 100% detectable polycystic ovary, and transabdominal 30% of patients are missed. For patients with unmarried obesity, anal ultrasound can be used for detection. In 1986, Adams first reported that the ultrasound of the ovary of PCOS patients showed that there were more than 8 follicles with diameter <10 mm in both ovaries, arranged along the periphery. With the increase of the central interstitial region, the polycystic ovary is usually enlarged, but there are also normal-sized polycystic ovaries. The ultrasound phase of PCOS patients can also be normal.

5, CT, MRI can also be used for ovarian morphology examination.

Diagnosis and identification of polycystic ovary syndrome

First, hormone determination

(A) gonadotropin: about 75% of patients with elevated LH, FSH normal or decreased, LH / FSH 3.

(B) steroid hormone

1. Androgen, including testosterone, dihydrotestosterone, androstenedione and 17 ketosteroids. The free androgen is elevated due to the decrease in SHBG.

2, the total amount of estrogen can reach 140pg / ml, androgen equivalent to the early stage of follicles about 60pg / ml, the formation of extragonadal estrone increased E1/E2 1.

3, the adrenal DHEAS production increased, plasma concentration 3.3g / ml, 17 hydroxyprogesterone also increased (normal <200ng / dL), if 800ng / dl should be considered delayed type congenital adrenal hyperplasia, 21 hydroxylation Enzyme or 11 hydroxylase deficiency. If it is 200 ~ 800ng / dl, it should be ACTH test (Cotrosyn 0.25mg iv) 60 minutes after the injection of 17 hydroxyprogesterone is congenital adrenal hyperplasia.

(C) Prolactin (PRL): about 25 to 40% of patients 25 ng / ml.

(4) Insulin (insulin); fasting insulin increased 14mu/L, IGF-I increased (normal 120mmol/L), plasma IGF-I binding protein decreased (normal <300ng/mL).

(5) Proopiomelancortin (POMC) and its derivatives: -lipotropin, -endorphin and -MSH are elevated, and ACTH is normal or elevated. TSH and GH are normal.

Hormone change

Too much androgen is a basic feature of polycystic ovary syndrome. Polycystic ovary syndrome can also have a significant increase in hormones including testosterone, free testosterone, andrographic acid, LH, LH/FSH ratio, free female Alcohol, estrone and fasting insulin. Hormone changes androgen excess is a basic feature of polycystic ovary syndrome. Polycystic ovary syndrome can also have a significant increase in hormones including testosterone, free testosterone, andrographic acid, LH, LH/FSH ratio, Free estradiol, estrone and fasting insulin.

Second, ultrasound examination

Bilateral ovarian polycystic enlargement, thickened echo of the capsule. There are a large number of visible under the capsule, and there are more than 10 capsules on one side or both sides of the cystic follicle with a diameter of 2 to 9 mm. Around the edge of the ovary, arranged in a wheel shape, called the necklace sign. Ovarian interstitial echo is uneven, endometrial hypertrophy, should be noted to exclude uterine and ovarian tumors and adrenal lesions.

Third, retroperitoneal angiography and hysterosalpingography

Objective To observe the morphology and size of ovary and adrenal gland to identify the causes of hyperandrogenism.

Fourth, diagnosis and endometrial disease examination

For patients 35 years old, routine diagnosis and endometrial examination should be performed to understand the histological changes of the endometrium (glandular cyst / adenoma / dysplasia) and exclude endometrial cancer.

Fifth, the endoscope

Including edema mirrors and laparoscopy to directly observe ovarian morphology or to perform biopsy, puncture, wedge cutting and electrocautery.

Sixth, CT and magnetic resonance

To identify and exclude pelvic tumors.

Seven, laparotomy

It is performed when a ovarian tumor is to be diagnosed or when an ovarian wedge is to be performed.

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